Psoriasis is a common, chronic, and relapsing skin disease characterized by hyperproliferation of keratinocytes and apoptosis delay. However, the molecular mechanisms underlying the progression of psoriasis remain elusive. MicroRNAs (miRNAs) are single-stranded, small non-coding RNAs that play a crucial role in the development of psoriasis by promoting targeted mRNA degradation or translational inhibition. Here, we report that miR-214-3p, one of the downregulated miRNAs identified in the skin of psoriatic patients and imiquimod (IMQ)-induced mouse models, can negatively regulate the expression of forkhead box M1 (FOXM1). miR-214-3p inhibition leads to hyperproliferation and increased apoptosis of keratinocytes in vitro. Moreover, we show that miR-214-3p inhibition causes an arrest of the cell cycle at the S stage by elevating the expression of NEK2, KIF20A, CENP-A, CENP-F, and Cyclin B1 and by reducing the expression of Cyclin D1 in HaCaT cells. In vivo, the administration of miR-214-3p attenuates the psoriasis-like phenotype in IMQ-induced mice. Collectively, our results suggest that miR-214-3p/FOXM1 axis in keratinocytes could be a novel target in the treatment of psoriasis.

银屑病是一种常见的慢性复发性皮肤病，其特征是角质形成细胞过度增殖和细胞凋亡延迟。然而，银屑病进展的分子机制仍然难以捉摸。MicroRNA (miRNA) 是单链、小的非编码 RNA，通过促进靶向 mRNA 降解或翻译抑制，在银屑病的发展中起关键作用。在这里，我们报告了 miR-214-3p 是在银屑病患者和咪喹莫特 (IMQ) 诱导的小鼠模型中发现的下调 miRNA 之一，它可以负调节叉头盒 M1 (FOXM1) 的表达。miR-214-3p 抑制导致体外角质形成细胞过度增殖和凋亡增加. 此外，我们发现抑制 miR-214-3p 通过提高 NEK2、KIF20A、CENP-A、CENP-F 和 Cyclin B1 的表达以及通过降低 Cyclin D1 的表达导致细胞周期停滞在 S 期。在 HaCaT 细胞中。在体内，施用 miR-214-3p 可减弱 IMQ 诱导的小鼠的银屑病样表型。总的来说，我们的结果表明角质形成细胞中的 miR-214-3p/FOXM1 轴可能是治疗银屑病的新靶点。